The long-term goal of these studies is to understand human cortical mechanisms of the sensory and affective dimensions of acute and chronic pain. Little is known about human cortical structures receiving nociceptive input; the role of attention in modulating input to these structures; or the functions of these cortical structures. Also, the human thalamic nuclei or cortical gyri where lesions lead to the development of central pain or where hyperactivity occurs in patients with central pain have not been clearly defined. Preliminary evidence indicates that potentials evoked by a pure pain stimulus are localized over human anterior cingulate cortex (ACC) and parasylvian cortex, which suggests that these areas receive nociceptive inputs. Lesions of the parietal operculum are associated with deficits of pain discrimination (sensory-discriminative aspect of pain) while lesions of the insula tend to be associated with deficits of the motivation to escape from painful stimuli (affective-motivational aspect of pain). The present study is designed to determine whether the human ACC, postcentral gyrus and parietal operculum receive nociceptive input. Cortical activity will be monitored over ACC, parasylvian and paracentral cortex during cutaneous stimulation with a carbon dioxide laser (laser evoked potentials - LEP) in epileptic patients with implanted subdural grids (Aim I). Stimulation with the laser evokes a pure pain sensation by selective activation of cutaneous nociceptors. The function of these nociceptive inputs will be assessed by psychophysical studies of patients with lesions of thalamus and cortex, but without central pain, to test the hypothesis that ACC and insula contribute to the affective aspect of pain while parietal operculum and SI contribute to the sensory aspect of pain (Aim II). LEPs will determine whether the lesions involve structures which receive nociceptive input. The hypothesis that lesions of pain and temperature signaling pathways result in central pain syndromes by producing increased activity of cortical areas normally receiving input from those pathways will then be tested (Aim III). PET studies will determine cortical areas that are hyperactive in response to stimuli which produce allodynia. These studies have unique potential to clarify the identity, function and pathophysiology of pain-signaling structures in human cortex.